Novel Mechanism Behind Autoimmunity Development Found

A new study from the National Institutes of Health (NIH) in the U.S. has led to the identification of a mechanism in the immune systems of mice that can lead to the development of autoimmune disease when inactivated.

Dr. Marko Pesu of the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) says that the findings shed light on the processes that lead to the development of autoimmunity, and could also have implications for the development of drugs to increase the immune response in diseases such as cancer and HIV.

Systemic Lupus Erythematosus (SLE) - Causes, Symptoms, Diagnosis and Treatment
Systemic Lupus Erythematosus (SLE) is an autoimmune disease that affects multiple organs like the joints, skin, kidney, heart, lungs, blood vessels and brain.

He joined forces with experts at the National Institute of Allergy and Infectious Diseases (NIAID) to study immune system T cells - specifically the helper T cell, an immune system component that helps other cells fight infection.

The researchers focused on the protein furin, an enzyme that plays an important role in the functioning of T cells.

With the aid of Belgium scientists, the research team created a mouse without furin only in T cells.

Unwanted �Ambulance Response� Of Immune Cells Can Be Blocked
A collaborative study has found a new way to selectively block the ability of white blood cells to ‘crawl’ toward the sites of injury and infection when such mobility drives disease.

The researchers observed that mice lacking furin in these cells developed systemic autoimmune disease, suggesting that the immune systems of the mice attacked their own cells and tissues throughout their bodies.

"We already know that furin seems to have roles in a variety of human diseases, such as cancer, cystic fibrosis and infectious diseases. These findings show that having no furin in certain immune system cells can increase the immune response and lead to autoimmune disease in mice," says Dr. Pesu.

Lupus Linked to Gene Mutation
Scientists at the Oklahoma Medical Research Foundation have identified a gene mutation that may cause the immune system to remain active even after fighting an infection, and thus

The study revealed that deleting furin in helper T cells affected the functioning of two types of T cells - regularoty cells that promote immune tolerance to the body's own cells and tissues, and effector cells.

The researchers further observed that mice lacking furin in regularoty T cells had lower levels of a specific protein, TGF-ß1, which is important for their ability to preserve immune tolerance.

Genetic Glitch may Cause Lupus
A research team led by an Indian-origin scientist has found that lupus may be caused due to abnormal editing of gene messages in a type of white blood cell.

However, they noted that effector T cells also produce TGF-ß1, and found that furin was also needed for TGF-ß1 production by effector T cells, and that its absence in effectors makes these cells more aggressive in causing autoimmune disease and tissue damage.

"Inhibiting furin has been thought to reduce growth of malignant cells or to block infections by preventing essential activation of a pathogen. However, these results suggest that the development of drug interventions could have an unexpected side effect of increasing the risk of developing autoimmune disease," says study author and NIAMS' Scientific Director John J. O'Shea, M.D., chief of the NIAMS' Molecular Immunology and Inflammation Branch.

Source-ANI
RAS/L